BE MOBILE 1 and BE MOBILE 2 are double-blind, phase 3 trials designed to evaluate efficacy and safety of bimekizumab, a novel dual interleukin (IL)-17A and IL-17F inhibitor, across the axial spondyloarthritis spectrum. touchIMMUNOLOGY were delighted to speak with Dr Fabian Proft (Charité Universitätsmedizin Berlin, Germany) about these trials and his poster on the maintenance of stringent clinical responses through one year of treatment with bimekizumab in patients with axial spondyloarthritis in phase 3 studies.
The abstract ‘Bimekizumab Maintained Stringent Clinical Responses Through Week 52 in Patients with Axial Spondyloarthritis: Results From the Phase 3 Studies BE MOBILE 1 and BE MOBILE 2 Poster‘ was presented at the European Alliance of Associations for Rheumatology (EULAR), 31 May – 03 June 2023.
Questions
- What is bimekizumab and what is its mechanism of action? (0:24)
- What were the primary and secondary endpoints of BE MOBILE 1 and BE MOBILE 2 and how well were they achieved? (1:20)
- What will be the likely place of bimekizumab in the treatment paradigm for axial spondyloarthritis? (3:37)
- What were the key take home messages from your poster at EULAR 2023? (4:40)
Disclosures: Fabian Proft discloses consultancy fees and speakers bureau from AbbVie, AMGEN, BMS, Eli Lilly, Hexal, Janssen, Medscape, MSD, Novartis, Pfizer, Roche & UCB and research support from Novartis, Eli Lilly and UCB.
Support:Â Interview and filming supported by Touch Medical Media Ltd. Interview conducted by Shanice Allen.
Filmed in coverage of the European Alliance of Associations for Rheumatology (EULAR) Annual Meeting
Click here for more content from EULAR.
Transcript
Hello everyone! My name is Fabian Proft, and I’m a rheumatologist working at the Charité University Hospital in Berlin, Germany. It is a pleasure for me today to speak about the abstract that I just recently represented at the EULAR 2023 in Milan.
What is bimekizumab and what is its mechanism of action?Â
Bimekizumab is a monoclonal IgG1 antibody that selectively inhibits IL-17F in addition to IL-17A, which are the two key cytokines involved in the pathobiology of spondyloarthritis. And what we know is that this additional inhibition of IL-17F, in addition to IL-17A, which we already know from secukinumab and ixekisumab, also makes a clinical difference, as we have seen in psoriasis patients in a head-to-head study, where the bimekizumab IL-17A and F inhibition, clearly outperformed IL-17A inhibition with secukinumab. Therefore, we are eagerly awaiting the approvals for axial spondyloarthritis and psoriatic arthritis to treat our patients in the nearer future.
What were the primary and secondary endpoints of BE MOBILE 1 and BE MOBILE 2 and how well were they achieved?
When speaking about BE MOBILE 1 and BE MOBILE 2, it’s utterly important to understand which patients haven’t been assessed in these trials and why we can, from my perspective, combine those studies together. Because BE MOBILE 1, non-radiographic axial spondyloarthritis, and then BE MOBILE 2, radiographic axial spondyloarthritis, formerly known as ankylosing spondylitis, were investigated. This makes the whole study project as a general axial spondyloarthritis project and, therefore, I think it’s very important to look at this as one study with two rather subpopulations. And here, the ASAS40 response after 16 weeks of treatment versus placebo was investigated and the primary results have just been fully published in Annals of Rheumatic Disease and showed clear superiority for both subgroups, in the non-radiographic and radiographic axial spondyloarthritis cohort, over placebo. And, when also looking at this data, the treatment onset, the rapid treatment onset, was really surprising or really benefiting for our patients. And also those patients that were then switched after 16 weeks of placebo treatment on the treatment with bimekizumab, they also had a very rapid treatment response after the switch. And, therefore, I think that we can very much look forward to have bimekizumab in the treatment armamentarium for treating our axial spondyloarthritis patients, and also, when looking at the two cohorts of non-radiographic in the BE MOBILE 1 and radiographic in the BE MOBILE 2, we don’t see any differences in the treatment response rates and, what was really fascinating when we were looking at those patients that have been previously been treated with another biological DMARD, with a TNFi, and those being bDMARD naive, there was no significant difference in the response rates indicating that those treatment modalities could really be an option also for those that have shown previous bDMARD failure.
What will be the likely place of bimekizumab in the treatment paradigm for axial spondyloarthritis?Â
This is a question that is not easy to answer at this stage because we are still lacking head-to-head data. But what we can already say when looking at the study data that we’ve just published, the BE MOBILE 1 and 2 phase 3 data, when cross-comparing this with other approval trials, phase 3 trials from the existing treatment modalities available in axial spondyloarthritis, we can assume that bimekizumab is at least as efficacious as the already available drugs. But we have, as already discussed, the clear superiority on skin manifestation of psoriasis, when compared to the currently best available treatment, the secukinumab. This means if I have a patient with axial spondyloarthritis and also psoriatic skin disease, I think this would be the ideal patient to be treated with bimekizumab in the nearer future in the clinic.
What were the key take home messages from your poster at EULAR 2023?Â
In this analysis, we examined the maintenance of stringent clinical response through one year of treatment with bimekizumab and patients with non-radiographic and radiographic access bar from both the BE MOBILE 1 and 2 study. And what we could show is that bimekizumab provided robust maintenance of stringent clinical response and low level of disease activity from week 16 to week 52 onwards across the whole disease spectrum of axial spondyloarthritis, meaning that from those patients that had a very good treatment response after 16 weeks of treatment, 90% of those patients were roughly also having the same treatment response rate at week 52.
Subtitles and transcript are autogenerated.